Syndecan-1 Laktat dan Profil Lipid sebagai Faktor Risiko Keparahan dan Mortalitas Sepsis

Yopie Wiguna; Philia Setiawan; Bambang Pujo Semedi; Bambang Purwanto

doi:10.15851/jap.v9n1.2251

Syndecan-1 Laktat dan Profil Lipid sebagai Faktor Risiko Keparahan dan Mortalitas Sepsis

Yopie Wiguna, Philia Setiawan, Bambang Pujo Semedi, Bambang Purwanto

Abstract

Pada sepsis, endothelial glycocalyx (EG), dapat rusak dan luruh melepaskan syndecan-1 ke dalam plasma. Kerusakan EG akan mengganggu mikrosirkulasi, menimbulkan hipoperfusi jaringan, dan meningkatkan kadar laktat. Gangguan profil lipid pada sepsis terjadi karena gangguan metabolisme dan kerusakan langsung hepatosit akibat meluruhnya EG. Penelitian ini bermaksud menganalisis syndecan-1, laktat, dan profil lipid sebagai faktor risiko keparahan dan mortalitas pada pasien sepsis. Penelitian ini adalah penelitian analitik observasional pada 39 pasien dewasa yang memenuhi kritera sepsis-3. Keparahan sepsis diklasifikasikan menjadi sepsis dan syok septik dan ditentukan dalam 6 jam setelah time zero berdasarkan penggunaan vasopresor, kecukupan resusitasi cairan, dan nilai laktat ulangan. Kematian 7 hari dihitung sejak time zero sepsis. Syndecan-1, laktat, dan profil lipid diambil dalam jam pertama setelah time zero dianalisis sebagai faktor risiko keparahan dan mortalitas 7 hari. Analisis data dilakukan dengan uji logistik regresi bivariat dan multivariat. Pada penelitian ini didapatkan 20 pasien dengan sepsis, 19 pasien dengan syok septik. Berdasar atas mortalitas 7 hari, 10 pasien meninggal dan 29 pasien bertahan hidup. Laktat dan syndecan-1 merupakan prediktor keparahan pada sepsis. Laktat merupakan variabel yang lebih superior dibanding dengan syndecan-1 sebagai prediktor keparahan sepsis. Laktat merupakan prediktor untuk mortalitas 7 hari pada pasien sepsis. Simpulan penelitian ini adalah laktat dan syndecan-1 merupakan prediktor keparahan pada sepsis. Laktat merupakan prediktor kematian 7 hari pada sepsis.

Syndecan-1 Lactate and Lipid Profiles as Risk Factors for Severity and Mortality in Sepsis

In sepsis, endothelial glycocalyx (EG) may experience damages and decay, releasing syndecan-1 into plasma. EG damages will disrupt microcirculation, causing tissue hypoperfusion and increasing lactate levels. Disorders of the lipid profile in sepsis occur due to metabolic disorders and direct hepatocyte damages due to EG shedding. This study intended to analyze the Syndecan-1, lactate, and lipid profiles as risk factors for severity and mortality in septic patients. This was an observational analytic study on 39 adult patients who met the criteria for sepsis-3. Sepsis severity was classified into sepsis and septic shock and was determined within 6 hours after time zero based on the vasopressor use, adequacy of fluid resuscitation, and repeat lactate values. The 7-day mortality was counted from time zero sepsis. Syndecan-1, Lactate, and Lipid Profiles were assessed within the first hour after time zero and analyzed as risk factors for severity and 7-day mortality. Data analysis was performed using bivariate and multivariate logistic regression tests. In this study, there were 20 patients with sepsis, 19 patients with septic shock. Based on the 7-day mortality, 10 patients died and 29 patients survived. Lactate and Syndecan-1 are predictors of severity in sepsis. Lactate is superior than Syndecan-1 as a predictor of sepsis severity and is a predictor of 7-day mortality in septic patients. Nonetheless, both lactate and Syndecan-1 are predictors of severity in sepsis.

Keywords

Keparahan sepsis, laktat, mortalitas 7 hari, profil lipid, sepsis, syndecan-1

Full Text:

PDF

References

Fleischmann C, Scherag A, Adhikari N, Hartog C, Tsaganos T, Schlattmann P, dkk. Assessment of global incedencce and mortality of hospital-treated sepsis. Current estimates and limitations. Am J Respirat Crit Care Med. 2016;193(3):259–72.

Vincent J, Nelson D, WIlliams M. Is worsening multiple organ failure the cause of death in patient with severes sepsis in the United States. Crit Care Med. 2011;39:1050–5.

Coletta C, Modis K, Olah G, Brunyanszki A, Herzig D, Sherwood E. Endothelial dysfunction is a potential contributor to multiple organ failure and mortality in aged mice subjected to septic shock: preclinical studies in a murine model of cecal ligation and puncture. Crit Care. 2014;18:511–3.

Chappell D, Jacob M. Role of the glycocalyx in fluid management: small things matter. Best Pract Res Clin Anaesthesiol. 2014;28:227–34.

Woodcock T, Woodcock T. The revised starling equation and the glycocalyx model of transvascular fluid exchange: an impeoved paradigm for prescribing intravenous fluid therapy. Br J Anaesth. 2012;108:384–94.

Rhodes A, Evans L. Surviving Sepsis Campaign: International Guidelines for Management of Septic and Septic Shock: 2016. Crit Care Med. 2017;45(3):1–67.

Ostrowski S, Berg R, Windelov N, Meyer M, Plovsing R, Moller K, dkk. Coagulopathy, cathecolamines, and biomarkers of endothelial damage in experimental human endotoxemia and in patients with severe sepsis: a prospective study. J Crit Care. 2013;28(5):586–96.

Cirstea M, Wailey K, Russell J, Brunham L, Genga K, Boyd J. Decreased high-density lipoprotein cholesterol level is an early prognostic marker for organ dysfunction and death in patients with suspected sepsis. J Crit Care. 2017;38:289–94.

Zou G, He J, Ren B, Xu F, Xu G, Zhang W. The delta high-density lipoprotein cholesterol ratio; a novel parameter for gram negative sepsis. Springer Plus. 2016;1044(5):1–12.

Oda K, Okada Hikeshi, Suzuki A, Tomita Hiroyuki. Factors enhancing serum syndcan-1 concentrations: a large comprehensive medical examination. J Clin Med. 2019;8:1320–30.

Tojo MY. Vaskular endothelial glycocalyx as a mechanism of vascular endothelial dysfunction and atherosclerosis. World J Cardiovasc Dis. 2020;10(10):1–19.

Adepu S, Katta K, Tietge U, Kwakernaak ADW, van Goor H, Navis G. Hepatic syndecan-1 changes associate with dyslipidemia after renal transplantation. Am J Transplantation. 2014;14(10):2328–38.

Yilmaz Y, Eren F, Colak Y, Senates E, Celikel C, Imeryuz N. Hepatic expression and serum levels of syndecan-1 in patients with nonalcoholic fatty liver disease. Scandinavian J Gastroenterol. 2012;47(12):611–6.

Anand D, Ray S, Srivastava L, Bhargava S. Evolution of serum hyaluronan and syndecan levels in prognosis of sepsis patients. Clin Biochemical. 2016;49:768–76.

Jones A. Should lactate clearacne be substituted for central venous oxygen saturation as goals of early severe sepsis and septic shock therapy?. Chest. 2011;140:1406–8.

Chien JY, Jerng JS, Yu CJ, Yang PC. Low serum level of high-density lipoprotein cholesterol is a poor prognostic factoir for severe sepsis. Crit Care Med. 2005;33(8):1688–93.

Pazzini A, Kurz K, Orth-Hoeller D, FIlle M, Lunger L, Tancevski I. The impact of bacteremia on lipoprotein concentrations and patient’s outcome: a retrospective analysis. J Clin Microbiol Infect Dis. 2019;2019:1–8.

Leeuwen H, Heezius E, Dallinga G, Strijp J, Verhoef J, Kessel K. Lipoprotein metabolism in patients with severe sepsis. Crit Care Med. 2003;31(5):1359–66.

Chelazzi C, Villa G, Mancinelli P, De Gaudio AR, Adembri C. Glycocalyx and sepsis-induced alterations in vascular permeability. Crit Care. 2015;19:1–7.

Mikkelsen ME, Miltiades AN, Gaieski DF, Goyal M, Fuchs BD, Shah CV, dkk. Serum lactate is associated with mortality in severe sepsis independent of organ failure and shock. Crit Care Med. 2009;37(5):1670–6.

Song JE, Kim MH, Jeong WY, Jung IY, Oh DH, Kim YC, dkk. Mortality risk factors for patients with septic shock afer implementation of the surviving sepsis campaign bundles. Infect Chemother. 2016;48(3):199–208.

Yealy D, Kellum J. ProCESS: a randomized trial of protocol based care for early septic shock. New Engl J Med. 2014;370:1683–93.

Lee SH, Park MS, Park BH, Jung WJ. Prognostic implications of serum lipid metabolism over time during sepsis. Biomed Res Internat. 2015;2015:1–8.

DOI: https://doi.org/10.15851/jap.v9n1.2251